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. 2014 Jan 13;111(4):1604–1609. doi: 10.1073/pnas.1315567111

Fig. 3.

Fig. 3.

MiR-17 regulates NSPC competence without altering the epigenetic status of the Gfap promoter. (A) MiR-17-OE p2 neurospheres did not undergo gliogenesis in response to LIF (10 ng/mL) and BMP2 (100 ng/mL) (n = 3). (Scale bar, 50 μm.) (B) The CpG methylation status of the Gfap promoter was analyzed by bisulfite sequencing. A total of 10 possible CpG cytosines in the Gfap promoter, including the CpG site in the STAT3-binding sequence (indicated by the arrows), were available for methylation. The percentages of methylated CpG cytosines in the Gfap promoter (Left) and the STAT3-binding region (Right) are shown (n = 5). (C) MiR-17 OE restored neuropotency in p3 neurospheres (n = 3). (Scale bar, 50 μm.) (D) The CpG methylation status of the Gfap promoter was analyzed by bisulfite sequencing, as described for B (n = 5). Results are shown as mean ± SEM. NS, P > 0.05; **P < 0.01.